Posterior myocardial infarction (MI)

#2021GM-JUL/Q21

Which part of the heart is 'posterior'?

Source
This article confirms that there is some confusion about which part of heart is the 'posterior' part.
Overall, it's the most posterior part of the wall in contact with the diaphragm.
That's segment 4 in the bull's-eye representation of the heart. (?used in CT)

• The "posterior wall" may not even exist. Source but it does for exam purposes.

What artery is inolved? See table above.

ECG changes in posterior MI

• ST depression in V1 - V4.
• ST segment elevation in V7,V8 and V9.
• Source

Source

• Posterior MI commonly occurs as a complication or extension of acute inferior STEMI.
  • Isolated posterior wall STEMI is uncommon.
• ST depressions occurs in the right precordial leads - V1,V2,V3 (along with inferior ST elevations due to the accompanying inf. STEMI).
  • STEMI patients who have dips in V1,V2 and V3 tend to have larger infarct sizes and higher risk of HF.
  • T waves in these leads are upright.
  • Tall R waves in V1 and V2 are reciprocals of Q waves in the posterior wall.
• The culpril artery is
  • Right coronary artery which perfuses the posterior wall by the posterior descending branch.
  • Or left circumflex artery.
    

Post MI prognosis

++ /dev/null

ECG features of myocardial ischemia

Source

1. ST elevation (>1mm)
2. ST depression - does not localise.
   1. ST depression confined to a single territory is likely to be reciprocal ST dips of an "opposite" ST elevation.
3. T inversion if
   1. At least 1 mm deep
   2. Present in ≥ 2 continuous leads that have dominant R waves (R/S ratio > 1)
   3. Dynamic — not present on old ECG or changing over time
4. Wellen's T waves

Features considered non specific for ischemia:
1. ST depression < 0.5 mm
2. T wave inversion < 1 mm
3. T wave flattening
4. Upsloping ST depression

STEMI diagnostic criteria

Source

De Winter T wave

• Is an ANTERIOR STEMI equivalent
• ST depression and peaked T in the precordial leads.
• 
• Highly specific for occlusion of the left anterior descending artery.
• like Wellen's sydndrome.
  • Peaked T - De Winder
  • Deep T - Wellens

Type 2 Myocardial Infarction

[!INFO] Definition of type 2 MI:
Myocardial infarction: Myocardial damage that occurs due to ischemia.

• Type 1 MI : MI due to acute atherothrombosis.
• Type 2 MI : MI due to supply demand mismatch without acute atherothrombosis thrombosis**.
  Source

Both must be differentiated from non-ischemic myocardial injury - i.e not an infarction.

[!INFO] Clinically distinguishing between Type 1 and Type 2 MI
The gold standard to distinguish between the two would theoretically be coronary angiography. However, in reality, it's a clinical judgement.

Presentation of type 2 MI

• Troponin values are usually lower than in type I MI but there is significant overlap. Source

• 

• Causes:

  • Hypertension (? increased afterload)
  • arrhythmias (eg tachyarrhythmias increase demand and decrease diastolic myocardial perfusion time)
  • infection
  • severe anemia
  • surgery
  • renal failure
  • and heart failure

• ECG features

  • ST segment changes cannot reliable differentiate type 1 from type 2.

Management of Type 2 MI

Management: See the image above.

Posterior myocardial infarction (MI)

#2021GM-JUL/Q21

Which part of the heart is 'posterior'?

Source
This article confirms that there is some confusion about which part of heart is the 'posterior' part.
Overall, it's the most posterior part of the wall in contact with the diaphragm.
That's segment 4 in the bull's-eye representation of the heart. (?used in CT)

• The "posterior wall" may not even exist. Source but it does for exam purposes.

What artery is inolved? See table above.

ECG changes in posterior MI

• ST depression in V1 - V4.
• ST segment elevation in V7,V8 and V9.
• Source

Source

• Posterior MI commonly occurs as a complication or extension of acute inferior STEMI.
  • Isolated posterior wall STEMI is uncommon.
• ST depressions occurs in the right precordial leads - V1,V2,V3 (along with inferior ST elevations due to the accompanying inf. STEMI).
  • STEMI patients who have dips in V1,V2 and V3 tend to have larger infarct sizes and higher risk of HF.
  • T waves in these leads are upright.
  • Tall R waves in V1 and V2 are reciprocals of Q waves in the posterior wall.
• The culpril artery is
  • Right coronary artery which perfuses the posterior wall by the posterior descending branch.
  • Or left circumflex artery.
    

Post MI prognosis

Treatment
Based in TSH level.

• If TSH > 10 mU/L -> treat with Thyroxine
• TSH between 4.5 and 10 -> treat on case by case basis.

• Streptococcus pneumoniae: Rust coloured sputum

• Clinically assessing the severity of an asthma exacerbation
• and when to give MgSO4. What are the possible side effects? What's the maximum dose?
• place for cough suppressants
• is T inversion and acute ischemic change?

• Fever patterns and differentials for each
• 
• what's a rational sequence for adding oral hypoglycaemics?
• why does ascitic tap cause encephalopathy? If isotonic fluid is removed from the abdomen, how can it promote more fluid leakage?
• why is esbl bad? Is it worse than MRSA
• what are the causes of bicytopaenia?
  • suspect a maha when there's a rapid haemoglobin drop with thrombocytopenia.
  • pregnancy is a common cause of ttp
  • sle is also a common cause of ttp. (There's something called autoimmune ttp).

pathogenesis of sciatica

- Beta blockers:  **propranolol** - given as first line locally, metoprolol (!? Even though it's cardioselective),

[[Myocardial infarction]]

Management of asthma:

Acute management of exacerbations

Source
See Source

[!INFO] Place for MgSO4
My initial question was whether MgSO4 is effective and safe and when it's use should be considered; At least in paediatrics, it's safe, effective, cheap and should be considered as first line parenteral therapy when initial management (with nebulisation) has failed. Use in preference to IV salbutamol infusion.
It works by multiple mechanisms including relaxing smooth muscle by blocking Ca entry and suppressing inflammation by 'stabilizing' immune cells.
Source

Asthma Vs. COPD

1. How to distinguish the two?
2. What are the significant differences in management?

[!INFO] Hypercapnia in asthma exacerbation is an alarming sign
Normally, there should be respriatory alkalosis;
Source

Source (2003 Article)

long term management

Goals of management

[!INFO] MPA and GPA are difficult to differentiate clinically
Because the staining patterns overlap
Source - lecture

https://careers.peninsulahealth.org.au/job/2024-PGY3%2B-Mid-Year-General-Stream-HMO/870-en_GB/
https://careers.peninsulahealth.org.au/job/2024-PGY3%2B-Mid-Year-General-Stream-HMO/870-en_GB/

MMRC